One aim of this research project is to characterize in detail the ionic flux and the current-voltage relations of the potassium inward rectifier in frog striated muscle fiber. The inward rectifier is located in the muscle membranes covering the external surface and those of the transverse tubular system. It is the major ionic pathway controlling the membrane potential and indirectly, other electrical properties of striated muscle under resting conditions. This rectifier system will be studied in cut single fibers under controlled membrane potentials where both the internal and external potassium ion concentrations can be varied. The effects of other alkali metal ions, such as rubidium and caesium, which both activate and block potassium movements through the rectifier will be studied. The modifications produced by various other agents such as hydrogen ions, barium, quaternary ammonium ions and various group specific chemical agents on this conductance system will also be studied. The entry of sodium and the loss of potassium through the inward rectifier is offset by the parallel action of the Na plus K plus exchange pump. Our other major aim is to better characterize this pump in skeletal muscle. The major fraction of the pump sites in muscle is located on the external surface and only a small fraction in the transverse tubular system. The Na[unreadable]+[unreadable] K[unreadable]+[unreadable] pump will also be studied in cut single fibers under controlled membrane potentials where the internal and external concentrations of both sodium and potassium can be varied as well as the levels of internal ATP and ADP. The parallel operation of these two systems determines the resting steady state distribution of Na plus and K plus and the resting membrane potential. The propertis of these systems are probably among the chief factors involved in hypotension and skeletal muscle weakness associated with hypokalemia and the paralysis of skeletal muscle associated with hyperkalemia.